Decreased expression of miR‑9 due to E50K OPTN mutation causes disruption of the expression of BDNF leading to RGC‑5 cell apoptosis

Mol Med Rep. 2016 Nov;14(5):4901-4905. doi: 10.3892/mmr.2016.5810. Epub 2016 Oct 6.

Abstract

The aims of the present study were to investigate the effect of E50K optineurin (OPTN) mutation on RGC‑5 cells and to define the role of microRNA‑9 (miR‑9) in this system. Transfected RGC‑5 cells were used to evaluate the effects of E50K OPTN on the expression of miR‑9 and subsequent disruption of RGC‑5 cell apoptosis was analyzed using western blotting. The results showed that the expression of E50K OPTN was associated with a marked reduction in the levels of miR‑9 in the E50K OPTN‑transfected RGC‑5 cells. The E50K OPTN‑dependent reductions in miR‑9 led to increased expression of the transcriptional repressor, RE1‑silencing transcription factor and decreased the expression of brain‑derived neurotrophic factor. Thus, E50K OPTN may disrupt the expression of miR‑9, suggesting a potential mechanism by which E50K OPTN mutation may lead to RGC‑5 cell apoptosis.

MeSH terms

  • Amino Acid Substitution
  • Apoptosis / genetics*
  • Brain-Derived Neurotrophic Factor / genetics*
  • Cell Cycle Proteins
  • Cell Line, Tumor
  • Codon
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Membrane Transport Proteins
  • MicroRNAs / genetics*
  • Mutation*
  • Neoplasms / genetics*
  • RNA Interference
  • RNA, Messenger
  • Repressor Proteins / genetics
  • Repressor Proteins / metabolism
  • Transcription Factor TFIIIA / genetics*
  • Transfection

Substances

  • Brain-Derived Neurotrophic Factor
  • Cell Cycle Proteins
  • Codon
  • MIRN92 microRNA, human
  • Membrane Transport Proteins
  • MicroRNAs
  • OPTN protein, human
  • RE1-silencing transcription factor
  • RNA, Messenger
  • Repressor Proteins
  • Transcription Factor TFIIIA